Defensive role of Nigella sativa against antituberculosis drugs induced renal toxicity.

Drug-induced nephrotoxicity is a common problem in clinical medicine and the frequency of drug-related acute and chronic kidney dysfunction worldwide. One of them is anti-tuberculosis (TB) drugs that cause renal function impairment during TB treatment. Medicinal plants contain bioactive compounds that are capable for treating drug or toxin-induced renal disorders. The aim of the present study was to assess the protective effect of the ethanolic extract of Nigella sativa seeds (NS) against anti-TB drugs (ATDs) induced nephrotoxicity in Wistar albino rats. Rats were treated with ATDs for 12weeks (3 alternative days in a week). Supplementation with 125mg NS/kg, p.o. was administered to the experimental rats for 12weeks (3 alternative days in a week considering next day of ATDs treatment). The results demonstrated that NS treatment protected against renal damage induced by ATDs, as evidenced by the reduction in serum urea, creatinine, uric acid, urea nitrogen levels, pro-inflammatory markers (TNF-α and IL-6), whereas improvement in histological tubular and glomerular damage. In addition, NS enhanced the antioxidant enzyme activity (superoxide dismutase and catalase) and decreased the lipid peroxidation and glutathione level in the kidney. In conclusion, NS could reduce chronic nephritis in ATDs treated group through suppressing inflammation and oxidative stress. It suggests that NS can be used as supplementary preventive and protective drug against kidney injury during anti-TB treatment.

Effect of electromagnetic radiation on redox status, acetylcholine esterase activity and cellular damage contributing to the diminution of the brain working memory in rats.

Behavioral impairments are the most pragmatic outcome of long-term mobile uses but the underlying causes are still poorly understood. Therefore, the Aim of the present study to determine the possible mechanism of mobile induced behavioral alterations by observing redox status, cholinesterase activity, cellular, genotoxic damage and cognitive alterations in rat hippocampus. This study was carried out on 24 male Wistar rats, randomly divided into four groups (n = 6 in each group): group I consisted of sham-exposed (control) rats, group II-IV consisted of rats exposed to microwave radiation (900 MHz) at different time duration 1 h, 2 h, and 4 h respectively for 90 days. After 90 days of exposure, rats were assessing learning ability by using T-Maze. A significantly increased level of malondialdehyde (MDA) with concomitantly depleted levels of superoxide dismutase (SOD), catalase (CAT) and redox enzymes (GSH, GPX, GR, GST, G-6PDH) indicated an exposure of mobile emitted EMR induced oxidative stress by the depleted redox status of brain cells. The depletion in the acetylcholinesterase (AChE) level reveals altered neurotransmission in brain cells. Resultant cellular degeneration was also observed in the radiation-exposed hippocampus. Conclusively, the present study revealed that microwave radiation induces oxidative stress, depleted redox status, and causes DNA damage with the subsequent reduction in working memory in a time-dependent manner. This study provides insight over the associative reciprocity between redox status, cellular degeneration and reduced cholinergic activity, which presumably leads to the behavioral alterations following mobile emitted electromagnetic radiation.

Mobile phone induced cognitive and neurochemical consequences.

With the rapid advances in technology, extensive use of mobile phones has increased the risk of health problems. This study was performed to find out the effect of mobile phone frequency on male Wistar rats. Animals were divided into two groups (n = 6 in each group). Group one was considered as control and group two (experimental group) was exposed to microwave radiation (2100 MHz) for 4 hours/day (5 days/week) for 3 months. Exposure of microwave radiation frequency showed significant alterations in cholinesterase activity, muscular strength, learning ability and anxiety. MWR exposure was also associated with significant alteration in the oxidative defense system and hippocampus degeneration. Histopathological observations clearly depicted the neural degeneration. Thus, it can be concluded that MWR significantly affects the central nervous system and may lead to many severe illnesses. This study may reveal a platform to understand its toxic effect and can further be used for amendment in current guidelines of mobile radiation.

Silver nanoparticles protect acetaminophen induced acute hepatotoxicity: A biochemical and histopathological approach.

The present study was premeditated to demonstrate the hepatoprotective effect of silver nanoparticles (AgNPs). Rats were treated with three different doses of AgNPs (50, 100 and 150 µg/kg, p.o.) after Acetaminophen (APAP; 2 g/kg, p.o. once only) intoxication. Treatment with AgNPs recouped the levels of serum aspartate amino transaminase (AST), alanine amino transaminase (ALT), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), bilirubin, triglyceride (TG) and cholesterol in dose dependent manner. Significant reduction in lipid peroxidation (LPO) and restoration of reduced glutathione (GSH) was found in liver in AgNPs treated animals. Alleviated activities of adenosine triphosphatase (ATPase), glucose-6- phosphatase (G6Pase) and antioxidant enzymes viz. superoxide dismutase (SOD) and catalase (CAT) due to APAP induced toxicity in liver were recovered by the treatment of AgNPs. Improvement in histoarchitecture of liver was also consistent with biochemical observations. The results revealed that AgNPs showed significant dose-dependent protection against APAP induced hepatocellular injury.

Therapeutic Efficacy of Nigella Sativa Linn. against Antituberculosis Drug-Induced Hepatic Injury in Wistar Rats.

Antituberculosis drug (ATD)-induced hepatotoxicity is a major impediment for the effective treatment of tuberculosis (TB). All first-line anti-TB medications have adverse effects that interrupt the successful completion of TB treatment. This investigation focuses on the evaluation of the protective role of Nigella sativa (NS) against liver injury caused by ATDs. Female rats were treated with ATDs for 8 weeks (3 d/wk) followed by NS for 8 weeks (3 d/wk). The antioxidant activity of NS was estimated with a 1,1-diphenyl-2-picrylhydrazyl (DPPH) assay and by analyzing total phenolic contents. Qualitative characterization of active compounds of the plant was done by high-performance liquid chromotography (HPLC). ATD-induced adverse effects were associated with sharp elevation in levels of serum transaminases, albumin, cholesterol, urea, uric acid, creatinine, and blood urea nitrogen (BUN). ATDs significantly increased lipid peroxidation (LPO) and decreased enzyme activities (superoxide dismutase [SOD], catalase [CAT], adenosine triphosphatase [ATPase], and glucose-6-phosphatase [G6Pase]) in liver, indicating oxidative stress. Conjoint treatment with NS could reverse the serological biochemistry and inhibit oxidative stress by suppressing LPO and augmenting antioxidant enzyme activity toward that of the control. Histological studies support the above biochemical findings. Results indicate that NS exerts excellent hepatoprotective abilities and can be used as a supplement to improve patient adherence and reduce interruptions in treatment due to ATD-related liver injury.

Lead acetate-induced hepatoxicity in Wistar rats: possible protective role of combination therapy.

Experimental studies have shown that sulphur-containing antioxidants have beneficial effects against the detrimental properties of Pb. In the present study, we investigated the therapeutic potential of combined administration of N-acetyl cysteine (NAC; 50 mg/kg p.o.) and selenium (Se; 0.5 mg/kg p.o.) against lead acetate intoxication (Pb; 0.2% in water ad libitum) in a male rat model for 12 wk. The exposure of rats to lead acetate produced significant (P < 0.05) alterations in cytochrome P450 (CYP) activity, microsomal lipid peroxidation, reduced glutathione, and proteins. In addition, significant elevation in liver markers transaminases, triglycerides, cholesterol, and bilirubin as well as a decline in albumin were also compared with the experimental control rats. Combined treatment of lead-exposed animals with NAC and Se showed marked improvement of the biochemical, molecular, and histopathological findings. These experimental results strongly indicate the protective effect of NAC alone with Se against toxic effects of lead on liver tissue.

Toxic effects of lead exposure in rats: involvement of oxidative stress, genotoxic effect, and the beneficial role of N-acetylcysteine supplemented with selenium.

This study was carried out to investigate the in vivo protective role of N-acetylcysteine (NAC) per se, along with selenium (Se), against lead-induced hepatic, nephritic-oxidative, and neuronal-oxidative damage in rats. Lead acetate at a dose of 50 mg/kg body weight administered intraperitoneally for 3 days was preferred as the source of lead. Various oxidative stress markers such as reduced glutathione content, lipid peroxidation, superoxide dismutase, and catalase were measured to determine the degree of oxidative damage and healing due to NAC (50 mg/kg body weight administered orally) and Se (0.5 mg/kg body weight administered orally) and were studied along with the activities of enzymes such as transaminases (aspartate aminotransferase/alanine aminotransferase), δ-aminolevulinic acid dehydratase, δ-aminolevulinic acid synthase, and acetyl cholinesterase activity. The genotoxic effect of lead also was studied in terms of DNA damage using comet assay. The effect of lead was studied in blood biochemical variables such as cholesterol, triglycerides, urea, uric acid, and creatinine. Our data suggest that supplementation of Se with NAC can improve the lead-induced biochemical oxidative stress in blood and tissue, the burden of lead on the body, and molecular alterations by recoupment in mean DNA damage.

Reversal of lead-induced toxicity due to the effect of antioxidants.

This study was designated to evaluate the protective effect of glutathione (GSH) and N-acetyl cysteine (NAC) in reducing the concentration of lead acetate in blood and soft tissues (liver, kidney, and brain) and their ability to restore altered hematopoietic, hepatic, renal, and other biochemical variables that are indicative of tissue oxidative stress in male rats. Male Wistar rats (150 ± 10 g) were randomly divided into 6 groups. Group 1 served as control. Group 2 served as experimental control was administered lead acetate (50 mg/kg intraperitoneally) for 3 days. Group 3 and 4 served as therapeutic controls. Animals in groups 5 and 6 received reduced GSH (1 mg/kg intraperitoneally) and NAC (50 mg/kg orally) for 3 days after the administration of lead acetate, as in group 2. The levels of hepatic and renal markers such as alanine aminotransferase, aspartate aminotransferase, triglycerides, cholesterol, urea, and uric acid were significantly increased (P ≤ 0.05) following administration of lead acetate. Administration of GSH and NAC provided significant protection to thiobarbituric acid reactive substances levels and reduced GSH content in tissues. On the other hand, significant recovery in lead-sensitive biochemical indices, like δ-aminolevulinic acid dehydratase, δ-aminolevulinic acid, and lead concentration in blood and soft tissues also were observed. It was concluded that NAC provided maximum protection compared with reduced GSH.